5.3 Endocrine and Metabolic Disorders
Key Takeaways
- Type 1 diabetes presents with polyuria, polydipsia, weight loss, and risk of DKA (fruity breath, Kussmaul respirations, anion-gap metabolic acidosis); type 2 is often insidious with obesity and insulin resistance
- Primary hypothyroidism shows high TSH with low free T4 (fatigue, cold intolerance, weight gain); primary hyperthyroidism shows suppressed TSH with high T4/T3 (weight loss, tremor, heat intolerance)
- Diabetic peripheral neuropathy causes burning, stocking-glove paresthesias that mimic radiculopathy — check glucose and HbA1c when neuropathic symptoms lack a clear nerve root pattern
- Hyperparathyroidism elevates calcium and PTH, causing bone pain, kidney stones, abdominal pain, and psychiatric symptoms ('stones, bones, abdominal groans, and psychic moans')
- Acute adrenal crisis (Addisonian crisis) presents with hypotension, hyponatremia, hyperkalemia, and shock — a medical emergency; chronic Cushing syndrome causes proximal myopathy, osteoporosis, and fragility fractures that contraindicate high-velocity manipulation
Why Endocrine Disease Matters on Part II
Endocrine and metabolic disorders rarely announce themselves with textbook labels. They walk in as fatigue, weakness, proximal myopathy, weight change, bone pain, paresthesias, and diffuse aching — the same language patients use to describe neuromusculoskeletal problems. NBCE Part II tests whether you can detect the systemic pattern inside a musculoskeletal-sounding history: the diabetic whose burning feet mimic L5 radiculopathy, the hypothyroid patient whose aching mimics fibromyalgia, the Cushing patient whose osteoporotic compression fracture is a manipulation hazard. Clinical impression starts with the endocrine differential when the whole-person picture does not fit a single spinal segment.
Diabetes Mellitus
Type 1 diabetes mellitus results from autoimmune destruction of pancreatic beta cells, causing absolute insulin deficiency. Onset is typically acute in children and lean young adults with polyuria, polydipsia, polyphagia, and unintentional weight loss. The life-threatening complication is diabetic ketoacidosis (DKA): hyperglycemia (>250 mg/dL), anion-gap metabolic acidosis, ketonemia, dehydration, Kussmaul respirations (deep, rapid breathing), and fruity breath from acetone. DKA is triggered by infection, missed insulin, or new-onset type 1.
Type 2 diabetes mellitus involves insulin resistance with relative insulin deficiency. Onset is insidious, often in overweight adults over 45, and may be discovered incidentally. Diagnosis: fasting glucose ≥126 mg/dL on two occasions, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5% (reflecting ~3 months of glycemic control). Prediabetes: fasting glucose 100–125 mg/dL or HbA1c 5.7–6.4%.
Hypoglycemia (<70 mg/dL) presents with diaphoresis, tremor, confusion, and irritability — common with sulfonylureas or insulin overdose. Severe hypoglycemia causes seizures and coma. Treat with oral glucose if alert; IV dextrose or IM glucagon if unconscious.
| Feature | Type 1 DM | Type 2 DM | DKA |
|---|---|---|---|
| Onset | Acute, young | Insidious, adult | Acute decompensation |
| Body habitus | Often lean | Often overweight | Any type 1 patient |
| Insulin | Absolute deficiency | Resistance + relative deficiency | Severe deficiency |
| Key labs | Anti-GAD antibodies | HbA1c elevated | Glucose high, pH low, ketones + |
Diabetic complications relevant to chiropractic triage: peripheral neuropathy (stocking-glove burning, numbness, loss of proprioception — increased fall and foot ulcer risk), autonomic neuropathy (orthostatic hypotension, gastroparesis), nephropathy (proteinuria progressing to ESRD), and retinopathy. Any patient with unexplained neuropathic symptoms needs glucose screening.
Thyroid Disorders
The thyroid gland regulates metabolism through T4 and T3; TSH from the pituitary is the best initial screening test.
Primary hypothyroidism (Hashimoto thyroiditis is the most common cause): high TSH, low free T4. Symptoms: fatigue, weight gain, cold intolerance, constipation, bradycardia, dry skin, coarse hair, and proximal muscle weakness/aching that mimics myopathy. Severe hypothyroidism → myxedema coma (hypothermia, altered mental status, respiratory depression).
Primary hyperthyroidism (Graves disease — autoimmune; toxic nodular goiter): suppressed TSH, elevated T4/T3. Symptoms: weight loss despite increased appetite, tremor, heat intolerance, tachycardia/atrial fibrillation, anxiety, and proximal weakness. Exam: diffuse goiter, exophthalmos (Graves), pretibial myxedema. Thyroid storm is the life-threatening extreme: fever, agitation, cardiovascular collapse.
Secondary (pituitary) hypothyroidism: low TSH AND low T4 — the pituitary fails to stimulate the thyroid. Do not confuse with primary hypothyroidism, where TSH is high.
| Pattern | TSH | Free T4 | Impression |
|---|---|---|---|
| Primary hypothyroidism | High | Low | Thyroid gland failure |
| Primary hyperthyroidism | Low | High | Thyroid overactivity |
| Secondary hypothyroidism | Low | Low | Pituitary failure |
| Subclinical hypothyroidism | High | Normal | Early thyroid failure |
Adrenal Disorders
Primary adrenal insufficiency (Addison disease) destroys the adrenal cortex, causing deficiency of cortisol and aldosterone. Features: fatigue, weight loss, hyperpigmentation (especially buccal mucosa and palmar creases), salt craving, hypotension, hyponatremia, and hyperkalemia. Acute adrenal crisis adds vomiting, abdominal pain, fever, and shock — triggered by infection or stress in an undiagnosed or undertreated patient. This is an emergency requiring IV hydrocortisone and fluids.
Cushing syndrome (excess cortisol — exogenous steroids, adrenal adenoma, pituitary ACTH adenoma) presents with central obesity, moon facies, buffalo hump, purple striae, hypertension, hyperglycemia, and proximal muscle weakness. Osteoporosis and fragility fractures (especially thoracic compression fractures) are common — high-velocity spinal manipulation is contraindicated until the metabolic cause is addressed.
Hyperaldosteronism (Conn syndrome): hypertension with hypokalemia (muscle weakness, cramps) and metabolic alkalosis. Suspect when hypertension is resistant to standard therapy.
Calcium, Bone, and Metabolic Disease
Primary hyperparathyroidism (parathyroid adenoma) elevates PTH and serum calcium. Classic mnemonic: "stones, bones, abdominal groans, and psychic moans" — kidney stones, bone pain/osteoporosis, constipation/pancreatitis, depression/confusion. Hypophosphatemia may accompany hypercalcemia. Surgical parathyroidectomy is curative.
Hypoparathyroidism (post-thyroid surgery): low calcium, high phosphate, tetany, Chvostek sign (facial twitch with facial nerve tap), Trousseau sign (carpal spasm with BP cuff inflation).
Osteoporosis: bone mineral density T-score ≤−2.5 on DEXA. Risk factors: postmenopausal women, corticosteroid use, hyperthyroidism, malabsorption. Presents with fragility fractures (wrist, hip, vertebral compression) after minimal trauma. Chiropractic care may proceed with modified techniques when osteoporosis is known, but acute compression fracture with neurologic deficit requires medical management.
Gout results from monosodium urate crystal deposition. Acute attack: sudden excruciating monoarticular pain and swelling, classically the first metatarsophalangeal joint (podagra), with redness and warmth. Risk factors: male sex, alcohol, diuretics, renal insufficiency, hyperuricemia. Diagnosis confirmed by joint aspiration showing needle-shaped, negatively birefringent crystals under polarized light. Chronic tophaceous gout forms subcutaneous tophi. Pseudogout (calcium pyrophosphate) affects larger joints (knee) with rhomboid, positively birefringent crystals.
Chiropractic Triage and Referral Red Flags
Refer before adjusting when you suspect:
- DKA or thyroid storm (altered mental status, Kussmaul breathing, fever with tachycardia and agitation)
- Adrenal crisis (hypotension, hyponatremia, hyperkalemia, shock)
- Severe hypoglycemia (altered consciousness)
- Hypercalcemic crisis (confusion, severe dehydration, calcium >14 mg/dL)
- Unexplained proximal weakness with systemic symptoms (endocrine myopathy)
- Known osteoporosis/Cushing with acute vertebral pain and possible fracture
- Neuropathic symptoms without dermatomal correlation — screen for diabetes
Endocrine disease changes the clinical impression from "mechanical back pain" to "systemic metabolic disorder with musculoskeletal manifestations." Part II rewards candidates who integrate labs (glucose, HbA1c, TSH/T4, calcium/PTH) with the history pattern.
Exam Tip
When a vignette lists fatigue, weight change, and diffuse aching without focal neurologic deficit, work through the endocrine differential (thyroid, adrenal, diabetes) before defaulting to fibromyalgia or somatic dysfunction. The abnormal lab value in the stem is almost always the key to the correct answer.
A 19-year-old man presents with polyuria, polydipsia, weight loss, and Kussmaul respirations. Arterial blood gas shows pH 7.18 with an elevated anion gap. The most likely clinical impression is:
Laboratory results show TSH 0.1 mIU/L (low) and elevated free T4. Which condition best explains this pattern?
A 58-year-old woman has fatigue, constipation, cold intolerance, and diffuse aching. TSH is 18 mIU/L and free T4 is low. Before treating her musculoskeletal complaints, the priority is:
A 52-year-old man has recurrent kidney stones, bone pain, constipation, and mild depression. Serum calcium and PTH are both elevated. The most likely diagnosis is: